Absolute blood eosinophil count and 1-year mortality risk following hospitalization with acute heart failure.

OBJECTIVE: In acute heart failure (AHF), hemoglobin, red cell distribution width, mean platelet volume, leukocytes, and relative lymphocyte count have been associated with mortality. It is not known whether absolute blood neutrophil, eosinophil, and monocyte counts are mortality predictors. METHODS: One hundred and seventy-six patients hospitalized due to AHF were enrolled. Treatment modalities and comorbidities influencing leukocyte counts were excluded. Hemogram, pro-brain natriuretic peptide, D-dimer, biochemistry, thyroid hormones, sensitive C-reactive protein, and echocardiography were obtained. Cardiovascular deaths during the first year after hospitalization were determined. RESULTS: Leukocyte and absolute neutrophil count were significantly higher and absolute lymphocyte count and absolute eosinophil count (AEC) were significantly lower in deceased patients than patients who survived. Groups were similar in terms of monocyte counts. BMI albumin, estimated glomerular filtration rate, free T3, ejection fraction were significantly lower, and ferritin, uric acid, D-dimer, pro-brain natriuretic peptide were significantly higher in deceased patients. Mitral regurgitation, hypotension, hyponatremia, and acute renal failure were also significantly more frequent among the deceased group. Binary logistic regression analysis employing significant variables showed that lower BMI, lower ejection fraction, hyponatremia, lower free T3, and lower AEC were independent predictors of death and as a whole were responsible from 81.8% of cardiovascular deaths. Death rate among patients with an AEC of 0.02 n/l×10 or less was 4.4-fold higher than patients with an AEC of more than 0.02 n/l×10. CONCLUSION: AEC of AHF patients measured at admission was found to be a stronger predictor of mortality than all other hemogram parameters and this is consistent with the increased sympatho-adrenal activity theory.

Oxidative stress and autonomic nervous system functions in restless legs syndrome.

BACKGROUND: Oxidative stress has been implicated in over 100 disorders in recent years; however, the situation in restless legs syndrome (RLS) has not been studied yet. METHODS: Fifty patients with RLS not medicated for RLS and 50 sex- and age-matched, healthy controls and controls with no pathology except mild iron deficiency or iron deficiency anaemia were enrolled. Patients with secondary RLS other than iron deficiency were excluded. Total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), arylesterase (ARE), paraoxonase (PON), stimulated paraoxonase (stim-PON), lipid hydroperoxides (LOOHs), acetyl cholinesterase (AChE) and butyryl cholinesterase (BuChE) were measured. Heart rate variability (HRV) analysis was performed. RESULTS: TOS, ARE and AChE were increased (P = 0·018, P < 0·001 and P < 0·001, respectively), whereas LOOHs were decreased (P < 0·001) in RLS group. TAS, OSI, PON and stim-PON were comparable. Erythrocyte sedimentation rate (ESR) and mean platelet volume (MPV) were increased (P = 0·021 and P = 0·037, respectively) in RLS group. HRV triangular index (HRVi) was lower (P = 0·012) in RLS group. Other HRV parameters were similar. CONCLUSIONS: Increased AChE and decreased LOOHs, which were influenced by increased PON1, were considered as indicators of efforts towards the protection of dopaminergic activity in central nervous system in RLS group. Increased ESR, MPV and low HRVi indicate elevated sympathetic activity in RLS group. Elevated sympathetic activity might be beneficial in relieving RLS symptoms, also causing increases in TOS. The evidence we found regarding oxidative stress and autonomic nervous system might be seminal in RLS treatment.

Prevalence of gluten sensitive enteropathy antibodies in restless legs syndrome.

The prevalence of restless legs syndrome (RLS) is increased in gluten sensitive enteropathy (GSE); but prevalence of GSE is not known in RLS. 96 RLS patients and 97 healthy controls, both with or without iron deficiency were enrolled. All secondary RLS patients except iron deficiency were excluded. Subjects underwent a thorough biochemistry and routine blood analyses, and tissue transglutaminase antibodies (TTGA), endomysium antibodies (EMA) and gliadin antibodies (AGA) were also tested. In RLS patients positivity rates of all GSE antibodies were similar to those in controls. The rate of iron deficiency anaemia in RLS patients with at least one positive GSE antibody was significantly higher than that of RLS patients whose GSE antibodies were all negative. The prevalence of GSE antibodies in RLS patients is not increased. GSE might have a role in the aetiology of RLS in association with iron deficiency anaemia. Since the prevalence of GSE antibodies is not increased in RLS, it seems unlikely that GSE is involved in the aetiology of RLS through different mechanisms (e.g. immunological mechanisms) other than iron deficiency as proposed in some published papers.

Splenomegaly in primary antiphospholipid syndrome without accompanying portal hypertension or comorbidity.

OBJECTIVE: To demonstrate the presence of splenomegaly in primary antiphospholipid syndrome (PAPS) patients without accompanying portal hypertension or comorbidity. METHODS: Twelve patients (7 women) aged 23-65 years followed upon the diagnosis of PAPS were enrolled in the study. We documented the identified causes of splenomegaly in patients with PAPS, and searched for the potential causes of splenomegaly in patients with spleen enlargement. PAPS patients with or without splenomegaly were evaluated in terms of demographic and clinical findings. RESULTS: Splenomegaly was present in 6 of the 12 patients. In these patients, there were no infections, hematological disorders, portal hypertension or malignancy that might lead to splenomegaly. The long axis of spleen was found to be in the range of 137-155 mm in patients with splenomegaly. Splenomegaly was more frequently determined in female PAPS patients. The splenomegaly group had a longer duration of disease (median 5.5 vs. 0.75 years) and a higher number of thrombotic events (median 3 vs. 1.5). The splenomegaly group was especially composed of patients who never received any anticoagulant and acetylsalicylic acid, or who used these agents irregularly for very short periods. CONCLUSION: Splenomegaly was observed in association with disease duration, frequency of thrombotic events and irregular antiaggregant or anticoagulant treatment in patients with PAPS, in the absence of comorbidity or portal hypertension.